Tumor derived EVs are classically viewed as a way to alter tumor microenvironment to facilitate cancer progression via the transfer of proteins such as: (i) epidermal growth factor receptor-vIII, an oncogenic receptor (119); (ii) multidrug resistance-associated protein 1 a membrane protein mediating export of organic anions and drugs from the cytoplasm (120); (iii) pro-angiogenic proteins, i.e., TGF-β and VEGF, etc. (121). This evidence concerns the gene VEGFA and neoplasm.